Delayed administration of zingerone mitigates the behavioral and histological alteration via repression of oxidative stress and intrinsic programmed cell death in focal transient ischemic rats

The neuronal mitochondria succumb to ischemia–reperfusion injury and release huge amount of reactive oxygen species and ultimately lead the neurons to intrinsic pathway of programmed cell death (iPCD). The present study was undertaken to elucidate the ischemia–reperfusion-induced oxidative stress an...

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Published in:Pharmacology, biochemistry and behavior biochemistry and behavior, 2013-11, Vol.113, p.53-62
Main Authors: Vaibhav, Kumar, Shrivastava, Pallavi, Tabassum, Rizwana, Khan, Andleeb, Javed, Hayate, Ahmed, Md. Ejaz, Islam, Farah, Safhi, Mohammed M., Islam, Fakhrul
Format: Article
Language:English
Subjects:
Animals
Apaf-1
Apoptosis - drug effects
Bax
Bcl-2
Behavior
Behavior, Animal - drug effects
Brain Ischemia - metabolism
Brain Ischemia - pathology
Brain Ischemia - physiopathology
Caspase
Enzyme-Linked Immunosorbent Assay
Guaiacol - administration & dosage
Guaiacol - analogs & derivatives
Guaiacol - pharmacology
Ischemia–reperfusion
Male
Oxidative Stress - drug effects
Rats
Rats, Wistar
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Summary:The neuronal mitochondria succumb to ischemia–reperfusion injury and release huge amount of reactive oxygen species and ultimately lead the neurons to intrinsic pathway of programmed cell death (iPCD). The present study was undertaken to elucidate the ischemia–reperfusion-induced oxidative stress and molecular events in iPCD 24h post ischemia–reperfusion injury and plausible mitigation by zingerone, a potent antioxidant of ginger rhizome. The right middle cerebral artery was occluded for 2h followed by reperfusion for 22hours. A maximum infarct volume (43.29%) and mitochondrial injury (56.99%) was observed in middle cerebral artery occlusion (MCAO) group. However, zingerone administration (50 and 100mg/kg b.wt. orally twice) at 5h and 12h from initiation of MCAO showed a significant reduction in infarct volume and mitochondrial injury (p
ISSN:0091-3057
1873-5177
DOI:10.1016/j.pbb.2013.10.008